Dectin-1, a myeloid type II C-type lectin family member, is the receptor for β-1,3 or -1,6-linked glucans (β-glucans) (Taylor et al., 2002), the important cell wall components of fungi. Genetic deficiency of Dectin-1 in both mice and human result in markedly excessive susceptibility to distinct species of fungi (Ferwerda et al., 2009; Saijo et al., 2007; Taylor et al., 2007), demonstrating the critical role of Dectin-1 in protecting the host from fungal infections. Through activating caspase recruitment domain-containing protein 9—nuclear factor kappa B pathway, Dectin-1 induces reactive oxygen species and proinflammatory cytokine production in dendritic cells (DCs) and macrophages (Mφ) and subsequently Th17 immune response (Conti et al., 2009; LeibundGut-Landmann et al., 2007). Nature-derived β-glucans are generally believed to have the effect on boosting host immunity and are widely used as food additives, but the accurate function of Dectin-1 signaling on mucosal immune system of gastrointestinal tract is still largely unknown.
Enteric microbiota balance plays a critical role in intestinal disease and health. Although several studies reveal that commensal fungi also exist in mammalian intestines (Iliev et al., 2012; Ott et al., 2008; Scupham et al., 2006), members of the domain bacteria dominate the trillions of microbes contained in human distal gut, and perform a variety of functions that benefit the host (Berg, 1996; Bjorksten et al., 2001; Martin and Rhodes, 2000; Umesaki and Setoyama, 2000). The mucosal immune system, developing along with the microbiota, obtains dual character of capacities which comprise both toleration of microbial components and defense of invading pathogens. Through receptors for pathogen-associated molecular pattern (PAMP), such as Toll-like receptors and nucleotide-binding oligomerization-domain protein-like receptors, enterocytes or Paneth cells sense bacterial pathogens and subsequently produce mucus and antimicrobial peptides (AMPs) to provide a protective barrier (Janeway and Medzhitov, 2002; Petnicki-Ocwieja et al., 2009; Vaishnava et al., 2008; Vaishnava et al., 2011), while intestinal phagocytes detect and response to luminal bacterial pathogens by inducing protective IgA or cytokines (Lande et al., 2007; Macpherson and Uhr, 2004; Niess et al., 2005). As a member of PAMP receptors, C-type lection receptor Dectin-1 is rarely studied on its function to intestinal immune cells and its influence to gut microorganism.
Recent studies show that a single special genus of intestinal commensal bacteria can influence the adoptive intestinal immunity and subsequently the intestinal or autoimmune diseases. By inducing RORγt+ Th17 cell differentiation, segmented filamentous bacteria (SFB) can promote experimental autoimmune encephalomyelitis or autoimmune arthritis (Lee et al., 2011; Wu et al., 2010), while by enhancing Foxp3+ Treg cell development, Clostridium can suppress chemically induced colitis (Atarashi et al., 2011). Functions on immune system by other potential commensal bacteria, however, have not been clarified yet.